![]() ![]() The two most commonly used objective methods of determining AFV include measurement of the maximum vertical pocket depth and the summation of the depths of the largest vertical pocket in each quadrant, or the AFI.Doppler ultrasound could be used to assess placental insufficiency, if suspected. Fetal growth should be checked to exclude intrauterine growth restriction leading to oliguria.During ultrasound, normal-appearing fetal kidneys and fluid-filled bladder may be observed to rule out renal agenesis, cystic dysplasia and ureteral obstruction.Suspicion of oligohydramnios may be prompted by discrepancies in sequential fundal height measurements, or by fetal parts that are easily palpated through the maternal abdomen.It may be discovered incidentally during routine scanning, or noted during antepartum surveillance for other conditions. The diagnosis is confirmed by ultrasound. ![]() Other maternal risk factors (including hypertension and diabetes) should also be assessed. Test for systemic lupus erythematosus (causes immune-mediated infarcts in the placenta and placental insufficiency). Drug-induced causes include indometacin and angiotensin-converting enzyme (ACE) inhibitors.Diabetes (either pre-existing or gestational diabetes).Twin-to-twin transfusion syndrome (monochorionic twins).It complicates as many as 12% of pregnancies that last beyond 41 weeks. Oligohydramnios is more common in pregnancies beyond term, as the AFV normally decreases at term. Oligohydramnios is a complication in approximately 4.4% of all pregnancies and severe oligohydramnios is a complication in 0.7% of pregnancies. Decreased fetal renal blood flow and decreased fetal urine production have been demonstrated beyond 42 weeks in pregnancies involving oligohydramnios.The decreased efficiency of placental function has been proposed as a cause but this has not been confirmed histologically.The cause of decreased AFV in post-term pregnancies is unknown.Anuria and oliguria lead to oligohydramnios.In growth-restricted fetuses, chronic hypoxia results in shunting of fetal blood away from the kidneys to more vital organs.As a sequela of hypoxaemia-induced redistribution of fetal cardiac output.Decreased renal perfusion leading to reduced urine production:.Fetal urinary tract malformations, including renal agenesis, cystic dysplasia and ureteral atresia. ![]()
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